Background: Perinatal stress is thought to underlie the Barker sequelae of low birth weight, of which precocious pubarche may be a manifestation. Aims: To explore whether prematurity as well as smallness for gestational age (SGA) predisposes to precocious pubarche, and the potential role of excess weight gain during childhood. Methods: Retrospective chart review of 89 children (79 girls) with precocious pubarche. Results: Sixty five per cent were overweight/obese at diagnosis, compared with 19–24% of Australian children. Thirty five per cent had a history of SGA and 24% of prematurity. Weight SDS increased from birth to diagnosis in 91% of children. The mean change in weight SDS from birth to diagnosis was greater in those who were SGA (2.8, 95% CI 2.2 to 3.4) versus AGA (1.7, 95% CI 1.3 to 2.2), with no difference in the incidence of overweight/obesity. The latter was lower among children born premature (40% versus 72% term) but was associated with a mean increase in weight of 1.3 SDS during childhood. Nine out of ten girls and boys with precocious pubarche had at least one of the three risk factors studied. Conclusions: Both prematurity and SGA were associated with precocious pubarche, as was overweight/obesity, irrespective of size or gestation at birth. Excess weight gain in childhood may predispose to precocious pubarche in susceptible individuals.

https://adc.bmj.com/content/archdischild/90/3/258.full.pdf

Precocious pubarche is associated with SGA, prematurity, weight gain, and obesity

DHEA, DHEAS and PCOS.

Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders characterized by androgen excess, oligo-ovulation and polycystic ovaries. Although ovaries are the main source of increased androgens in the syndrome, between 20 and 30% of patients with PCOS have adrenal androgen (AA) excess, detectable primarily by elevated dehydroepiandrosterone sulfate (DHEAS) levels. Patients with PCOS demonstrate a generalized hypersecretion of adrenocortical products, basally and in response to ACTH stimulation. The mechanisms of these abnormalities are unclear although AA excess in PCOS is likely a complex trait, modulated by both intrinsic and acquired factors. To date, no specific genetic defects have been identified. The production of AAs in response to ACTH appears to be closely related to altered factors regulating glucose-mediated glucose disposal, increased peripheral metabolism of cortisol, and to a less extent to the effects of extra-adrenal androgens, insulin resistance, hyperinsulinemia or obesity. Finally, DHEAS levels and the response of AAs to ACTH are relatively constant over time and are closely correlated between PCOS patients and their siblings suggesting that this abnormality is an inherited trait in PCOS.

The adrenal and polycystic ovary syndrome.

Context: Polycystic ovary syndrome (PCOS) is the most common endocrinopathy affecting women of reproductive age. Hyperandrogenism is the central feature of PCOS. Studies on isolated ovarian theca-interstitial cells suggest that resveratrol, a natural polyphenol, reduces androgen production. Objective: This study was designed to evaluate endocrine and metabolic effects of resveratrol on PCOS. Design and Setting: This was a randomized (1:1) double-blind, placebo-controlled trial that evaluated the effects of resveratrol over a period of 3 months in an academic hospital. Patients and Other Participants: Subjects with PCOS were identified according to the Rotterdam criteria. Thirty-four subjects were enrolled and 30 subjects completed the trial. Evaluations were performed at baseline and repeated after 3 months of treatment. Intervention: Resveratrol (1,500 mg p.o.) or placebo were administered daily. Main Outcome Measure: Primary outcome was the change in the serum total T. Results: Resveratrol treatment led...

/pdf/effects-of-resveratrol-on-polycystic-ovary-syndrome-a-double-3ntpdm3ika.pdf

Effects of Resveratrol on Polycystic Ovary Syndrome: A Double-blind, Randomized, Placebo-controlled Trial.

Objectives: The risk of some cancers is positively associated with body weight, which may influence circulating levels of sex-steroid hormones, insulin and IGF-I. Interrelationships between these hormones and the associations with adiposity were evaluated in healthy women participating in the European Prospective Investigation into Cancer and Nutrition (EPIC). Methods: A cross-sectional analysis was performed on anthropometric and hormonal data from 743 pre- and 1217 postmenopausal women. Body mass index (BMI) and waist circumference were used as indicators of adiposity. C-peptide, Insulin Growth Factor (IGF)-I, Insulin Growth Factor binding protein (IGFBP)-3, androgens, estrogens and sex hormone binding globulin (SHBG) were measured by immunoassays; free sex steroid concentrations were calculated. Results: BMI and waist circumference were positively correlated with estrogens in postmenopausal women and with C-peptide, free testosterone and inversely with SHBG in all women. C-peptide and IGF-I were inversely correlated with SHBG, and positively with free sex steroids in postmenopausal women. IGF-I was positively associated with postmenopausal estrogens and androgen concentrations in all women. Conclusions: Sex-steroid concentrations appear to be regulated along several axes. Adiposity correlated directly with estrogens in postmenopausal women and with insulin, resulting in lower SHBG and increased levels of free sex steroids. Independent of adiposity and insulin, IGF-I was associated with decreased SHBG levels, and increased concentrations of androgens and postmenopausal estrogens.

/pdf/c-peptide-igf-i-sex-steroid-hormones-and-adiposity-a-cross-1cbzm29t5b.pdf

C-peptide, IGF-I, sex-steroid hormones and adiposity: A cross-sectional study in healthy women within the European Prospective Investigation into Cancer and Nutrition (EPIC)

https://www.fertstert.org/article/S0015-0282(01)02014-3/pdf

Elizabeth R Smith

Papers

Influence of insulin and testosterone on adrenocortical steroidogenesis in vitro: preliminary studies.